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PubMed2004

Implementation of guidelines for management of heart failure in heart failure clinic: effects beyond pharmacological treatment.

BACKGROUND: Patients with heart failure have scarce knowledge of their condition and frequently report poor quality of life. In spite of numerous studies showing improvement of survival and reduction in hospitalizations, several epidemiological studies showed that substantial proportion of patients are not receiving appropriate treatment. Intensive multidisciplinary approach can improve management of the patients with heart failure. AIM: To assess the efficacy of intensive patient management in heart failure clinic with respect to patient knowledge, pharmacological management, and quality of life. METHODS: From outpatients, visiting the heart failure clinic in period form March 2002 to March 2003, we prospectively enrolled patients with heart failure due to systolic dysfunction. Patient knowledge about their condition was assessed by a knowledge questionnaire. Data on their clinical characteristics, diagnostic and pharmacological management were analyzed. Quality of life was assessed with Minnesota Living with Heart Failure Questionnaire (MLHFQ). Patients rated their quality of life and heath on a seven-category descriptive scale from 1 (best) to 7 (worst). Data are shown as mean (S.D.). RESULTS: In this period we treated 50 patients (33 men), aged 67 (12) years. Patient knowledge about their condition improved after two visits to heart failure clinic (4.8 (1.5) vs. 7.3 (1.4), p<0.001). More patients were treated with beta blockers (40% vs. 84%, p<0.001) while there was a positive trend for treatment with angiotensin-converting enzyme inhibitors (94% vs. 98%) and spironolactone (54% vs. 70%). Equivalent mean daily dose of enalapril (11.0 (11.0) mg to 16.7 (8.7) mg, p<0.001) and carvedilol (13.0 (11.5) mg to 32.1 (18.2) mg, p<0.001) increased. Out-patient management was associated with improvement of MLHFQ score (47 (18) vs. 34 (16)), NYHA class (2.9 (0.4) vs. 2.5 (0.7)), quality of life score (5.3 (1.1) vs. 3.7 (1.0)), and health score (5.1 (1.1) vs. 3.7 (1.1)) (p<0.001 for all). CONCLUSIONS: Intensive management in heart failure clinic can be effective for translation of guidelines into clinical practice. It also improves patient's knowledge and quality of life as well as reduces the hospitalizations in heart failure patients.

Aged↗
PubMed2002

"Diastolic heart failure" or heart failure caused by subtle left ventricular systolic dysfunction?

OBJECTIVES: To determine whether patients with suspected heart failure but preserved systolic function, as determined by conventional echocardiographic measures (often said to have "diastolic heart failure), might have subtle left ventricular systolic dysfunction detectable by a new measure of left ventricular systolic function-left ventricular systolic atrioventricular plane displacement. DESIGN: Observational study. SETTING: Direct access echocardiography. PATIENTS: 147 patients with suspected heart failure referred by general practitioners. MEASUREMENTS: Echocardiographic assessment of conventional measures of left ventricular systolic function (fractional shortening, ejection fraction (by Simpson's biplane method) and "eyeball" assessment) and measurement of left ventricular systolic atrioventricular plane displacement. RESULTS: Between 21% and 33% of patients with "normal" left ventricular systolic function by conventional methods were found to have abnormal left ventricular systolic atrioventricular plane displacement. CONCLUSIONS: Approximately one quarter of patients with suspected heart failure but preserved systolic function by conventional methods have abnormal atrioventricular plane displacement. These patients with suspected heart failure but preserved systolic function by conventional echocardiographic measures may have heart failure caused by subtle systolic dysfunction rather than isolated "diastolic heart failure".

Aged↗
PubMedDate not supplied

Heart rate variability analysis in the assessment of autonomic function in heart failure.

Heart rate is not static, but rather changes continuously in response to physical and mental demands. In fact, an invariant heart rate is associated with disease processes such as heart failure. Heart rate variability analysis is a noninvasive technique used to quantify fluctuations in heart rate. In this article, the authors review neural control of heart rate, briefly describe heart rate variability, and summarize research data demonstrating that heart failure is associated with altered heart rate variability. In addition, the authors present evidence that heart failure patients with decreased heart rate variability are at risk for future cardiac events, heart transplantations, and death.

Baroreflex↗
PubMed2000

Meta-analysis of observed mortality data from all-controlled, double-blind, multiple-dose studies of losartan in heart failure. Losartan Heart Failure Mortality Meta-analysis Study Group.

Clinical studies of heart failure utilizing losartan, an angiotensin-II receptor antagonist, found that this drug is well tolerated and demonstrates hemodynamic, neurohormonal, and symptomatic improvement. To assess all-cause mortality in heart failure patients treated with losartan, a meta-analysis including 1,896 patients was performed on 6 controlled, double-blind, multiple-dose studies, regardless of sample size or duration of follow-up. A combination of logarithmic (log) odds ratios with a continuity correction was utilized for the meta-analysis. Treatment groups were comparable with regard to demographic characteristics, heart failure characteristics, and concomitant cardiovascular therapies. Concomitant use of open-label angiotensin-converting enzyme (ACE) inhibitors was not allowed in any study. The mean left ventricular ejection fraction obtained in individual studies ranged from 23% to 31%. Seven hundred forty patients were randomized to control therapy and 1,154 patients were randomized to losartan therapy. There were 36 deaths (3.12%) in the losartan groups compared with 47 in the control groups (6.35%) during the double-blind periods. The odds of dying in the losartan groups were 0.51 times (0.31 to 0.81) that of dying in the control groups (p = 0.004). In this analysis, treatment with losartan provided a beneficial effect upon survival. However, because the number of deaths in these studies is relatively small and the follow-up relatively short, a large confirmatory study is needed to assess the mortality benefit of losartan compared with an ACE inhibitor.

Adult↗
PubMed1999

Augmented short- and long-term hemodynamic and hormonal effects of an angiotensin receptor blocker added to angiotensin converting enzyme inhibitor therapy in patients with heart failure. Vasodilator Heart Failure Trial (V-HeFT) Study Group.

BACKGROUND: ACE inhibitors may not adequately suppress deleterious levels of angiotensin II in patients with heart failure. An angiotensin receptor blocker added to an ACE inhibitor may exert additional beneficial effects. METHODS AND RESULTS: Eighty-three symptomatic stable patients with chronic heart failure receiving long-term ACE inhibitor therapy were randomly assigned to double-blind treatment with valsartan 80 mg BID, valsartan 160 mg BID, or placebo while receiving their usual ACE inhibitor therapy. Studies were performed before and after the first dose of the test drug and again after 4 weeks of therapy. A single dose of lisinopril was administered during study days to ensure sustained ACE inhibition. Compared with placebo, the first dose of valsartan 160 mg resulted in a significantly greater reduction in pulmonary capillary wedge pressure at 3, 4, and 8 hours and during the prespecified 4- to 8-hour interval after the dose and in systolic blood pressure at 2, 3, 6, 8, and 12 hours and 4 to 8 hours after the dose. A pressure reduction from valsartan 80 mg did not achieve statistical significance. After 4 weeks of therapy, net reductions in 0-hour trough pulmonary capillary wedge pressure (-4.3 mm Hg; P=0. 16), pulmonary artery diastolic pressure (-4.7 mm Hg; P=0.013), and systolic blood pressure (-6.8 mm Hg; P=0.013) were observed in the valsartan 160 mg group compared with placebo. After 4 weeks of therapy, plasma aldosterone was reduced by valsartan 80 mg BID (-52. 1 pg/mL; P=0.001) and 160 mg BID (-47.8 pg/mL; P<0.001) compared with placebo, and there was a trend for a reduction in plasma norepinephrine (-97 pg/mL; P=0.10). Seventy-four of the 83 patients completed the trial. CONCLUSIONS: Physiologically active levels of angiotensin II persist during standard long-term ACE inhibitor therapy.

Aged↗
PubMedDate not supplied

Difficult cases in heart failure: Reversible heart failure secondary to thyrotoxicosis.

Perhaps one of the most important steps in caring for a patient with heart failure is seeking a reversible form of heart failure. Often addressing a disease process, like myocardial ischemia or systemic hypertension, rapidly attenuates the progressive natural history of left ventricular dysfunction. Beyond the usual reversible causes, however, are some that may be overlooked. This case provides an insight into one of these causes. (c)1999 by CHF, Inc.

Journal Article↗
PubMed2004

Severity of left ventricular remodeling defines outcomes and response to therapy in heart failure: Valsartan heart failure trial (Val-HeFT) echocardiographic data.

OBJECTIVES: The objective of this study was to test the hypothesis that the severity of left ventricular remodeling predicts the response to treatment and outcomes in chronic heart failure. BACKGROUND: Reversal of remodeling should produce the most favorable outcome in patients with the most severe remodeling. METHODS: In 5010 heart failure patients on background therapy and randomized to valsartan and placebo, serial recordings of left ventricular internal diastolic diameter (LVIDd) and ejection fraction (EF) were read at sites that had to meet qualifying standards before participating. Baseline LVIDd and EF were pooled across treatments and retrospectively grouped by quartiles Q1 to Q4, representing best to worst. Kaplan-Meier survival curves were obtained by the log-rank test. Q1 was compared with Q4 for mortality and combined mortality and morbidity (M + M) from Cox regression risk ratios (RRs). Valsartan versus placebo changes from baseline in LVIDd and EF were analyzed by quartiles from analysis of covariance. Valsartan and placebo were compared by RRs for M + M. RESULTS: Survival rates were greater in the better quartiles for LVIDd and EF (p < 0.00001). The RR for Q1 versus Q4 in events approached 0.5 for both LVIDd and EF (p < 0.0001). An LVIDd decrease and EF increase were quartile-dependent and greater with valsartan than placebo at virtually all time points. The RR for M + M outcomes favored valsartan in the worse quartiles. CONCLUSIONS: Stratification by baseline severity of remodeling showed that patients with worse LVIDd and EF are at highest risk for an event, yet appear to gain the most anti-remodeling effect and clinical benefit with valsartan treatment.

Antihypertensive Agents↗
PubMed2002

Hemodynamic and neurohumoral effects of selective endothelin A (ET(A)) receptor blockade in chronic heart failure: the Heart Failure ET(A) Receptor Blockade Trial (HEAT).

BACKGROUND: The endothelin (ET-1) system is activated in chronic heart failure (CHF). Whether, what type, and what degree of selective ET blockade is clinically beneficial is unknown. We investigated hemodynamic and neurohumoral effects of 3 weeks of treatment with various dosages of the orally available ET(A) antagonist darusentan in addition to modern standard therapy in patients with CHF. METHODS AND RESULTS: A total of 157 patients with CHF (present or recent NYHA class III of at least 3 months duration), pulmonary capillary wedge pressure > or =12 mm Hg, and a cardiac index < or =2.6 L x min(-1) x m(-2) were randomly assigned to double-blind treatment with placebo or darusentan (30, 100, or 300 mg/d) in addition to standard therapy. Short-term administration of darusentan increased the cardiac index, but this did not reach statistical significance compared with placebo. The increase in cardiac index was significantly more pronounced after 3 weeks of treatment (P<0.0001 versus placebo). Pulmonary capillary wedge pressure, pulmonary arterial pressure, pulmonary vascular resistance, and right atrial pressure remained unchanged. Heart rate, mean artery pressure, and plasma catecholamines remained unaltered, but systemic vascular resistance decreased significantly (P=0.0001). Higher dosages were associated with a trend to more adverse events (including death), particularly early exacerbation of CHF without further benefit on hemodynamics compared with moderate dosages. CONCLUSIONS: This study demonstrates for the first time in a large patient population that 3 weeks of selective ET(A) receptor blockade improves cardiac index in patients with CHF. However, long-term studies are needed to determine whether ET(A) blockade is beneficial in CHF.

Blood Pressure↗
PubMed2001

Pathogenesis of heart failure.

Heart failure is a complex clinical syndrome, and only part of this syndrome is based on the mechanical failure of the heart muscle itself to provide sufficient systemic perfusion. Heart failure is accompanied by the activation of various immunologic and neurohumoral mechanisms. These may be intended by nature to be physiologically beneficial, but eventually become deleterious as they provoke ischemic, proarrhythmic, vascular, and structural changes in the myocardium that contribute to the versatile symptoms of the heart failure syndrome. Today's concept of the pathogenesis of heart failure regards heart failure as a dynamic state influenced by at least 2 major mechanisms, namely "neurohumoral" activation and ventricular remodeling. Progressive chronic heart failure can be viewed as a result of the prolonged impact of both pathogenetic mechanisms. This article will describe briefly the features of the neurohumoral forces on the pathogenesis of heart failure, including immunologic forces, which also influence the remodeling process.

Animals↗
PubMed1990

Arterial baroreceptor control of peripheral vascular resistance in experimental heart failure.

Heart failure is known to impair arterial baroreceptor control of heart rate. To determine if baroreceptor control of peripheral vascular resistance is also impaired, heart rate and hind limb vascular responses to phenylephrine and nitroglycerin administration were compared in control dogs and in dogs with heart failure produced by chronic rapid ventricular pacing. Baroreflex control of the heart rate was depressed in the dogs with heart failure, as evidenced by a reduced slope of the blood pressure-to-heart rate relationship (controls: -2.5 +/- 0.3 beats/mm Hg versus heart failure: -1.5 +/- 0.2 beats/mm Hg [(p less than 0.04)]). Arterial blood pressure in the dogs with heart failure was also reduced (controls: 90 +/- 3 mm Hg versus heart failure: 75 +/- 3 mm Hg [(p less than 0.01)]). Nevertheless, dogs with heart failure exhibited normal slopes of the blood pressure versus hind limb vascular resistance relationship (controls: -2.4 +/- 0.4 units/mm Hg versus heart failure: -2.9 +/- 0.5 units/mm Hg [(p = NS)]), consistent with preserved baroreflex control of the peripheral vasculature. These data suggest that heart failure impairs arterial baroreflex control of heart rate and lowers the baroreflex pressure operating range but does not alter baroreflex control of peripheral resistance.

Animals↗
PubMed2006

The incidence of new onset congestive heart failure and heart failure exacerbation in Veteran's Affairs patients receiving tumor necrosis factor alpha antagonists.

The objective of this study was to evaluate the incidence of new onset or worsening congestive heart failure in Veteran's Affairs (VA) patients who have received infliximab, etanercept, or adalimumab, and to compare mortality rates in these patients to control populations. We enrolled three groups of patients for this retrospective study: TNF-alpha group (n = 103), a rheumatoid arthritis (RA) control group (n = 100), and a control group without RA (n = 100). All patients at our VA facility who had received at least one dose of the TNF-alpha antagonists were included in the TNF-alpha group. Admissions for CHF did not differ between the three groups: TNF-alpha 7 (6.7%), RA control 8 (8%), non-RA control 7 (7%); P = 0.940. Mortality rates were not significantly different: TNF-alpha 4 (3.8%), RA control 7 (7%), non-RA control 11 (11%); P = 0.147. Our study showed no difference between the three groups in either CHF exacerbation or mortality.

Adalimumab↗
PubMed1999

Drug-induced heart failure.

Heart failure is a clinical syndrome that is predominantly caused by cardiovascular disorders such as coronary heart disease and hypertension. However, several classes of drugs may induce heart failure in patients without concurrent cardiovascular disease or may precipitate the occurrence of heart failure in patients with preexisting left ventricular impairment. We reviewed the literature on drug-induced heart failure, using the MEDLINE database and lateral references. Successively, we discuss the potential role in the occurrence of heart failure of cytostatics, immunomodulating drugs, antidepressants, calcium channel blocking agents, nonsteroidal anti-inflammatory drugs, antiarrhythmics, beta-adrenoceptor blocking agents, anesthetics and some miscellaneous agents. Drug-induced heart failure may play a role in only a minority of the patients presenting with heart failure. Nevertheless, drug-induced heart failure should be regarded as a potentially preventable cause of heart failure, although sometimes other priorities do not offer therapeutic alternatives (e.g., anthracycline-induced cardiomyopathy). The awareness of clinicians of potential adverse effects on cardiac performance by several classes of drugs, particularly in patients with preexisting ventricular dysfunction, may contribute to timely diagnosis and prevention of drug-induced heart failure.

Adjuvants, Immunologic↗
PubMed2003

Pathophysiology of congestive heart failure.

Heart failure is a clinical syndrome characterized by impaired structure and/or function of the heart, leading to dyspnea and fatigue at rest or with exertion. The pathophysiology of heart failure is complex, and there is no single lesion. Any form of heart disease can lead to heart failure. Most heart failure can be explained by well-recognized etiologic factors, though ostensibly healthy patients may harbor risk factors for the later development of heart failure. A fundamental response to myocardial injury or altered loading conditions includes "remodeling" of the heart, so that the size, shape, and function of the affected chamber is grossly distorted. This is accompanied by a constellation of biologic changes, best recognized in advanced cases of heart failure. These multiple alterations may be primary or secondary events but, nonetheless, add importantly to the morbidity and mortality of the patients. More emphasis should be placed on recognition and correction of risk factors related to the development of heart failure.

Cardiomyopathy, Dilated↗
PubMed1998

Frequency of low-risk hospital admissions for heart failure.

Heart failure is one of the most common reasons for admission to acute care hospitals. A proportion of these admissions are probably low risk and could be managed in subacute care facilities, resulting in substantial cost savings. To investigate the proportion of low-risk hospital admissions for heart failure, all admissions for heart failure to Vanderbilt University Medical Center between July 1993 and June 1995 were identified (n = 743). One hundred twenty of these admissions were randomly selected, reviewed, and classified into a high-risk versus low-risk group on admission based on the severity of heart failure and the presence of life-threatening complications. Of the 120 admissions, 57 (48%) were classified as high risk based on the presence of moderate to severe heart failure for the first time or recurrent heart failure with a major complicating factor. Sixteen admissions (28%) were associated with adverse outcomes, including myocardial infarction in 5 (9%), intubation in 6 (11%), and death in 4 (7%). Sixty-three admissions (52%) were classified as low risk based on the presence of new-onset mild heart failure or mild to moderate recurrent heart failure with no complicating factors. Most of these admissions were for dyspnea without any life-threatening complication; 57 (91%) had no evidence of interstitial or alveolar pulmonary edema, and arterial oxygen saturation averaged 95 +/- 3%. Only 3 of these low risk admissions (5%) were associated with an adverse cardiovascular event. None of the patients died. These data suggest that over half of the patients admitted for heart failure to an acute care facility are low risk and probably could be managed in a subacute care setting, resulting in large cost savings.

Aged↗
PubMed2005

Respiratory-related heart rate variability in progressive experimental heart failure.

Heart failure is associated with autonomic imbalance, and this can be evaluated by a spectral analysis of heart rate variability. However, the time course of low-frequency (LF) and high-frequency (HF) heart rate variability changes, and their functional correlates during progression of the disease are not exactly known. Progressive heart failure was induced in 16 beagle dogs over a 7-wk period by rapid ventricular pacing. Spectral analysis of heart rate variability and respiration, echocardiography, hemodynamic measurements, plasma atrial natriuretic factor, and norepinephrine was obtained at baseline and every week, 30 min after pacing interruption. Progressive heart failure increased heart rate (from 91 +/- 4 to 136 +/- 5 beats/min; P < 0.001) and decreased absolute and normalized (percentage of total power) HF variability from week 1 and 2, respectively (P < 0.01). Absolute LF variability did not change during the study until it disappeared in two dogs at week 7 (P < 0.05). Normalized LF variability increased in moderate heart failure (P < 0.01), leading to an increased LF-to-HF ratio (P < 0.05), but decreased in severe heart failure (P < 0.044; week 7 vs. week 5). Stepwise regression analysis revealed that among heart rate variables, absolute HF variability was closely associated with wedge pressure, right atrial and pulmonary arterial pressure, left ventricular ejection fraction and volume, ratio of maximal velocity of early (E) and atrial (A) mitral flow waves, left atrial diameter, plasma norepinephrine, and atrial natriuretic peptide (0.45 < r < 0.65, all P < 0.001). In tachycardia-induced heart failure, absolute HF heart rate variability is a more reliable indicator of cardiac dysfunction and neurohumoral activation than LF heart rate variability.

Animals↗
PubMed1999

Heart failure.

Heart failure is predominantly a disorder of older adults, and to a large extent the epidemiology of heart failure reflects the convergence of age-related changes in the cardiovascular system and the rising prevalence of age-related cardiovascular diseases. The diagnosis of heart failure in the elderly is often difficult because of the presence of atypical symptomatology and comorbid conditions. Similarly, optimal treatment frequently poses a therapeutic challenge because of the high prevalence of confounding medical, behavioral, psychosocial, and economic factors. In addition, there is a paucity of data on the pharmacotherapy of heart failure in the very elderly (over age 80), and in the large proportion of older patients with heart failure and preserved left ventricular systolic function. Despite these difficulties, a number of therapeutic options, including ACE inhibitors, digoxin, and possibly beta blockers and angiotensin receptor antagonists, have been shown to favorably affect the clinical course of heart failure in elderly patients. In addition, several studies have documented the efficacy of multidisciplinary heart failure disease management programs for reducing hospital admission rates, improving quality of life, and decreasing cost of care. At present, the three greatest challenges in managing older heart failure patients are: (1) to more effectively implement proven treatments, such as ACE inhibitors, disease management systems, and antihypertensive therapy; (2) to develop effective therapies for the treatment of diastolic heart failure; and (3) to develop more effective means for heart failure prevention. It is hoped that future studies will address each of these critically important issues.

Aged↗
PubMed2000

Cardiac sympathetic afferent reflexes in heart failure.

Heart failure is characterized by an elevation in sympathetic tone. The mechanisms responsible for this sympatho-excitation of heart failure are not completely understood. Several studies from this laboratory have compared differences in the cardiac "sympathetic afferent" reflex between sham dogs and dogs with pacing-induced heart failure. We found 1) that the cardiac sympathetic afferent reflex is augmented in heart failure, 2) tonic cardiac sympathetic afferent inputs play an important role in the elevated sympathetic tone in heart failure, 3) cardiac sympathetic afferents are sensitized in heart failure and 4) the central gain of the cardiac sympathetic afferent reflex in heart failure is sensitized and that this sensitization may be related to augmented central Ang II and blunted NO mechanisms. These studies integrate into the regulation of sympathetic outflow in heart failure which is likely to be mediated by a variety of peripheral inputs modulated by central substances. If the cardiac sympathetic afferent reflex is one of the excitatory reflexes which contribute to sympathetic activation in heart failure, a comprehensive understanding of neuro-humoral regulation of this reflex may result in more definitives and rational therapy targeted to the sympathetic nervous system in this disease state.

Afferent Pathways↗
PubMedDate not supplied

Guidelines for the diagnosis and management of heart failure.

Heart failure has reached epidemic proportions. Five million Americans have been diagnosed with heart failure, and this number is expected to double within the next 30 years. One million patients are hospitalized annually with decompensated heart failure, and half will be readmitted for recurrent symptoms within 6 months. Heart failure primarily affects the elderly and is the most common reason for hospitalization in this age group. The prognosis for heart failure is poor, worse than most malignancies. Heart failure accounts for 280,000 deaths annually, and the 5-year survival rate is less than 50% despite multiple therapeutic advances. Poor survival may be attributed in part to poor application of evidence-based heart failure therapies and patient noncompliance. This review describes current guidelines for diagnosing and managing patients with heart failure.

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